Brain Health 1

Question 1

drugs v neurotransmitters

Answer 1

Neurotransmitters = chemicals that direct neuronal activity and behavior
Drugs = chemicals that mimic, enhance, or block the action of neurotransmitters

Question 2

classification of psychoactive drugs

Answer 2

Sedative Hypnotics and Anxiolytics
Antipsychotics
Antidepressants
Psychomotor Stimulants
Narcotic Analgesics
Psychedelics and Hallucinogens

Question 3

sedative hypnotics and anxiolytics

Answer 3

Examples: Alcohol, Barbiturates (anesthesia), Benzodiazepines (valium, xanax, etc), Ketamine
Effects: range from reduced anxiety to sleep to coma/death
NTs affected: GABA agonists

Question 4

tolerance

Answer 4

the diminished response to a drug over time, must take more and more to get the same initial effect.

Question 5

cross tolerance

Answer 5

someone who is tolerant to the effects of a certain drug also develops a tolerance to another drug.
Alcohol, Barbiturates, and Benzodiazepine show cross-tolerance because affect the same GABA receptor.

Question 6

fetal alcohol syndrome

Answer 6

Alcohol passes through the placenta and prevents enough nutrition and oxygen from getting to the fetus leading to:
(FAS is incurable)
Small brains and head, underdeveloped gyri and sulci, abnormal clusters of cells and misaligned cells in cortex, learning disabilities to mental retardation (poor language and math skills), hyperactivity, lack of focus, mood swings, abnormal facial features (smooth ridge between the upper lip and nose, small and wide-set eyes, very thin upper lip), below average height and weight, poor coordination, problems with vision and hearing, heart problems, kidney defects.

Question 7

psychosis

Answer 7

inability to discern between reality and delusions/hallucinations (can develop in people without schizophrenia)

Question 8

psychosis extras

Answer 8

Examples Neuroleptics: (older) Chlorpromazine, Haloperidol (Haldol), (newer) Clozapine, Zyprexa, Risperdal
Effects: reduce motor activity, reduce hallucinations and delusions, can cause Parkinsonian symptoms or tics (Older meds: dyskinesia -chewing movement, darting tongue, drooling, sedated, difficulty thinking)
NTs affected: Dopamine antagonists

Question 9

how do antipsychotics work

Answer 9

Antipsychotics work by binding to D2 receptors and blocking dopamine from binding so that the channel does not open.

Question 10

antidepressants

Answer 10

Examples: MAO inhibitors, Tricyclics, SSRI’s
Effects: reduction of anxiety/depression, possible sexual dysfunction, sedation, dry mouth, blurred vision, memory impairment
NTs affected: serotonin, norepinephrine, histamine, acetylcholine, dopamine agonists; mostly block destruction and reuptake of serotonin and norepinephrine

Question 11

psychomotor stimulants

Answer 11

All stimulants increase the activity of neurons in both the CNS and PNS. Also called “Uppers”.
Effects:
Enhances alertness, awareness, wakefulness, endurance, productivity and motivation, increases arousal, perception, locomotion, heart rate and blood pressure, diminishes requirement for food and sleep, improves mood, relieves anxiety, causes euphoria, racing speech and thoughts, paranoia

Question 12

three groups of psychomotor stimulants

Answer 12

General Stimulants
Behavioral Stimulants
Psychedelics

Question 13

general stimulants

Answer 13

Examples: Caffeine, Nicotine
Effects: enhances the activity of the nervous system, Caffeine – reduces drowsiness, increases alertness, enhances mood, improves energy output, increases relaxation and relieves depression but side effects are dizziness, irritability, nausea, and nervousness, headache with withdrawal Nicotine – euphoria and relaxation, alertness and arousal also causes lung cancer, seizures, chest pain, irregular heartbeat
NTs affected: Caffeine - adenosine antagonist but glutamate, dopamine, acetylcholine, and serotonin agonist Nicotine - acetylcholine agonist

Question 14

caffeine mechanism of action

Answer 14

Normally, Adenosine is a neuromodulator and when it binds to receptors, neural activity slows down facilitating sleep and dilating blood vessels for adequate oxygenation during sleep.
Caffeine blocks A2 adenosine G-protein coupled receptors which inhibit an enzyme that normally breaks down a second messenger, cAMP (cyclic adenosine monophosphate). As cAMP increases, more glucose is produced in the cell, which increases cell activity.
Caffeine activates the HPA axis - neural circuits signal the Pituitary gland to release ACTH which targets the Adrenal Glands to secrete adrenaline for burst of energy.

Question 15

caffeine tolerance

Answer 15

Regular caffeine intake leads to slight tolerance, withdrawal, and therefore dependency. First, the body will produce more adenosine receptors in response to too much caffeine, causing tolerance.

Question 16

Then, as caffeine is stopped:

Answer 16

Increased adenosine – blood vessels dilate, which causes headaches and nausea
Reduced serotonin – anxiety, irritability, inability to concentrate, decreased motivation, mild depression
Reduced dopamine – drowsiness and fatigue

Question 17

behavioral stimulants

Answer 17

Examples: Cocaine, Amphetamines, Methamphetamine
Effects: euphoria, increased alertness, elevation of mood and confidence, increased motor behavior and endurance, loss of appetite, addiction, brain damage, death, mania (Affects Pleasure Centers of the Brain)
NTs affected: dopamine, serotonin, norepinephrine agonists (blocks transporters for reuptake)

Question 18

cocaine mechanism of action

Answer 18

Brain areas affected: Nucleus accumbens and ventral tegmental area (centers for pleasure and reward), amygdala and hippocampus (centers emotions and memory), prefrontal cortex (center for weighing options and restraint)

Question 19

cocaine is addictive

Answer 19

New offshoots of dendrites produced in hippocampus, amygdala, and prefrontal cortex causes cravings from drug-associated memories.
Number of dopamine receptors decreases and less dopamine produced (downregulation)
Feel anxious, depressed and unable to feel normal pleasure without the use of cocaine; now addicted!

Question 20

Symptoms of Cocaine Addict:

Answer 20

loss of weight, trouble sleeping, extreme fatigue, nervousness, stereotypic behaviors (pacing), paranoia, cardiac and pulmonary abnormalities (irregular heartbeat), frequent infections.

Question 21

methamphetamine mechanism of action

Answer 21

Causes dopamine, serotonin, and norepinephrine to flood the synapse. Binds to Monoamine oxidase to prevent the breakdown of NT’s. Binds to transporters blocking reuptake and also reversing its action.

Question 22

meth is addictive

Answer 22

Loss of Dopamine transporters causes tolerance and greater use causes structural and functional damage to the brain: whole brain inflammation, reduced grey matter in hippocampus and limbic system, difficulty feeling pleasure, mood disturbances and violent behavior, hallucinations, paranoia, loss of cognitive abilities and memory, loss of motor abilities (Parkinson-like tremors), destruction of blood vessels and muscle tissue which inhibits the body’s ability to repair itself. Psychotic symptoms can last months to years after quitting.

Question 23

narcotic analgesics/opiates

Answer 23

Examples: Morphine, Codeine, Heroin, Vicodin, Oxycontin, Oxycodone, Percocet
Opium from poppy pod morphine synthesize heroin
Effects: sleep-inducing (narcotic), pain-reducing (analgesic), euphoria, potential addiction, brain damage, death (side effects: sleepiness, difficulty concentrating, blurry vision, poor night vision, slowed breathing, slight anxiety, nausea, vomiting, constipation, and poor appetite) Also called “Depressants” or “Downers”.
NTs affected: opioid/endorphin agonists

Question 24

heroin mechanism of action

Answer 24

Heroin modifies action of dopamine in reward centers of the brain (nucleus accumbens, ventral tegmental area).
Heroin is converted to morphine, powerful agonist at mu opioid receptors. Binding inhibits release of GABA, which can no longer tell a second neuron to decrease the release of dopamine, therefore a second neuron increases the release of dopamine into the synapse and the sustained action of dopamine produces the “high” or the euphoria felt.

Question 25

short term effects of heroin

Answer 25

Heroin mimics endorphins and binds to endorphin receptors causing feelings of intense pleasure “rush”, warm flushing of the skin, and sense of well-being.

Other symptoms: dizziness, feeling as though body is heavy, pleasantly drowsy, slurred speech, pupils constrict, eyelids droop, nausea, fatigue, ability to function both mentally and physically will decrease, slows breathing rate and heart rate sometimes to point of death.

Heroin is a “downer” and affects the brain’s ability to feel pain and the brain’s pleasure center.

Question 26

heroin long term

Answer 26

Long-term effects: Damage to the respiratory and cardiovascular systems (infection of heart lining and valves, collapsed veins), infections (HIV, Hepatitis B and C) and bacterial infections, abscesses (boils), arthritis and other rheumatologic problems, liver and kidney disease.
Severe withdrawal. Very Addictive! When the drug wears off, there is no protection against pain and the painful side effects are so strong that there is an extreme urge to use again. Seeking and using heroin becomes a person’s primary purpose in life.

Question 27

heroin withdrawal symptoms

Answer 27

Withdrawal is not life-threatening despite the tremendous discomfort but dope sickness leads to suicide. Withdrawal lasts 3 days to several weeks. Psychological cravings can last months to years.
Methadone and Buprenorphine do not provide the “high” but control the painful withdrawal symptoms so that user can be weaned off of heroin.

Question 28

how does naloxone prevent heroin death

Answer 28

Naloxone (Narcan) has stronger affinity and binds more strongly to opioid receptors than heroin, knocking the heroin off the receptor for a short time (may need to re-administer).

Question 29

psychedelics and hallucinogens

Answer 29

Examples: Mescaline, LSD, Marijuana, Mushrooms
Effects: altered sensory perception (colors may have sounds, sounds may have smells, separation from the body), altered cognition and confusion, hallucinations, paranoia, depression, nausea/vomiting, brain damage, “flashbacks”
NTs affected: agonists for acetylcholine (atropine), norepinephrine (mescaline), cannabinoids (marijuana), serotonin (LSD)

Question 30

marijuana mechanism of action

Answer 30

Many natural endogenous cannabinoid NT’s like anandamide, oleamide, 2-AG (2-arachidonylglycerol), bind to cannabinoid receptors in the cerebral cortex, hippocampus, basal ganglia, and cerebellum controlling thought, concentration, memory, time and depth perception, and coordinated movement.
THC (tetrahydrocannabinol) binds to cannabinoid receptors to interfere with the normal functioning of neurons and indirectly increases dopamine release leading to psychotropic effects. CBD (cannabidiol) indirectly is a serotonin agonist contributing to anxiolytic effects.

Question 31

effects of marijuana

Answer 31

Effects: altered sensory perception, heightened mood, feeling of well-being, relaxation, impaired short-term memory, impaired motor skills (reaction time), impaired judgment, lack of motivation, red eyes, increased heart rate, respiratory problems, and higher doses lead to mild hallucinations, paranoia, anxiety.
Beneficial effects: reduce nausea, stimulate appetite, reduce neuropathic pain, reduce seizures
Detrimental Effects in Adolescence: Disrupts brain development and changes the structure of the brain in areas for memory and problem solving, increased risk for mental health problems (depression, anxiety, schizophrenia in people with predisposition), greater likelihood of addiction.
Marijuana is Addictive, powerful psychological dependency. No known death from overdose.